Successful, efficient, sterile placement of intravenous (IV) catheters should be mastered by all providing care of the emergent patient. It should be understood that placement of short, large-bore peripheral catheters provide the most rapid means for intravascular volume expansion.
Successful, efficient, sterile placement ofintravenous (IV) catheters should be mastered by all providing care of the emergent patient. It should be understood that placement of short, large-bore peripheral catheters provide the most rapid means for intravascular volume expansion. However, venous cannulation may prove difficult in the hypovolemic, shocky patient. It must be remembered that hypovolemia decreases the pressure gradient between the arterial and venous systems, making aggressive manual venous occlusion a risk for impairing arterial flow to the limb and being counterproductive in providing venous engorgement. In this situation, a facilitating incision or mini-cutdown may prove helpful to properly visualize the vessel.
Placement of a peripherally inserted central catheter (PICC line) may be preferred in patients that require the administration of substances with increased osmolality (diazepam infusions, parenteral nutrition, dextrose supplemented fluids, etc), patients that require frequent blood sampling or those prone to severe bruising (thrombocytopenia). Standard through-the-needle catheters are prone to mechanical occlusion (kinking). Replacing the needle with a similar sized peripheral catheter offers an option that has proven to lower the risk for kinking. These catheters may be successfully placed in most common peripheral vascular sites, however, venous valves may provide added obstacles with full advancement of the central catheter.
Catheter-related bloodstream infections (CR-BSI) are a preventable cause of morbidity and mortality. Interventions that enhance provider awareness of CR-BSI, consolidate catheter equipment and supplies into a catheter cart or tote, confirm the continued need of catheters on a daily basis, and empower nurses to enforce adherence to evidence-based infection control practices have been shown to nearly eliminate CR-BSI in human intensive care units.
Whole blood components include red blood cells (RBCs), white blood cells (WBCs) platelets and plasma. Centrifugation of hematocrit tubes separates blood into plasma, packed RBC and a buffy coat (BC) layer. These parameters should be routinely evaluated in emergency patients that are having bloodwork performed and/or being started on intravenous fluid therapy. This information may provide rapid insight as to overall hydration status, total RBC mass, total protein levels (including albumin), condition of serum (lipemia, hemolysis, icterus, etc), and function as a weak indicator of elevated WBC or platelet numbers in the patient.
Acute hemorrhage causes a variety of alterations in the PCV/TS depending on the time from the initial insult. Beginning immediately after blood loss and continuing for 48-72 hours after blood loss, interstitial fluid moves into the vessels to replace the lost volume, decreasing PCV/TS values over time. Also in response to acute hemorrhage, the spleen contracts, releasing RBCs, but not protein. If the PCV/TS are measured soon after the onset of hemorrhage, the PCV will be normal or elevated, with a normal TS. As time progresses or when IV fluids are administered, the PCV and TS will decrease as the intravascular volume is replaced. With acute alterations, the PCV/TS should be measured frequently (ie. as often as every 30-60 minutes) to monitor for conditions requiring blood component therapy.
Alterations in hydration status will also alter the PCV/TS. They will increase or decrease simultaneously depending on whether water, not blood, is gained (over hydration) or lost (dehydration or hemoconcentration). Using the PCV/TS to assess hydration status often reveals a more severe dehydration than is assessed by mucous membrane moisture and skin turgor.
If only the PCV is low with normal TS, etiologies may include RBC destruction, decreased RBC production, or chronic cavitary hemorrhage. If the PCV is low to normal, with high TS, there may be an elevated globulin level or concomitant dehydration. If only the PCV is elevated along with a normal TS, look for conditions that cause dehydration or hemoconcentration masked by hypoproteinemia (hemorrhagic gastroenteritis) or an absolute increase in RBCs (polycythemia / erythrocytosis). If the PCV is elevated with low TS, suspect splenic contraction with pre-existing hypoproteinemia.
The provision of anesthesia is necessary for successful treatment of many emergency disorders. Although risks inherent to this patient population cannot be completely eliminated, care can be taken to limit this risk in a patient population that is more vulnerable to its associated complications (hypothermia, hypotension, hypoventilation, cardiopulmonary arrest, etc) through the proper administration of premedications and IV fluid support, in addition to proper utilization of anesthetic monitoring.
It is with rare exception, that anesthesia should be provided in the absence of systemic analgesics (primarily opioids, less frequently lidocaine or NSAIDs, rarely alpha2-agonists) ± sedatives (primarily benzodiazepines, rarely phenothiazine derivatives). Clinical conditions that may justify the administration of anesthesia without a premedication are those disorders where a rapid and full recovery from anesthesia is best for the patient. This becomes an invalid argument if the patient underwent a procedure that evokes a sustained painful stimulus upon awakening.
In addition to administering appropriate premedications and IV fluid support, anesthetic monitoring is imperative for a safe anesthetic period for the patient. There is no argument that multi-parameter monitoring is advocated for all anesthetic events lasting longer than the time it takes to instrument the patient. Although a pulse oximeter is probably the single most commonly used anesthetic monitoring modality, it provides the least amount of clinically useful information in a patient receiving 100% oxygen. Instead, both blood pressure monitoring and end-tidal carbon dioxide monitoring provide more clinically useful information, based on the rate of anesthetic complications that involve one of these parameters.
The administration of supplemental oxygen (O2) to an emergency patient is ultimately intended to help improve O2 delivery to the vital organs. The increased fraction of inspired O2 (FiO2) is intended to have a domino affect by increasing O2 content in the upper airways, lower airways, alveoli, pulmonary veins, systemic arterial tree, tissue interstitium and ultimately the cells.
Many respiratory patients are very anxious. Anxiety contributes to increased O2 consumption through added work of breathing and restlessness. Administration of anxiolytics (specifically butorphanol) helps limit this increased O2 consumption. By limiting oxygen "waste" through skeletal muscle consumption, more O2 is available for distribution to vital organs. Anxiolysis also allows the patient to tolerate O2 administration techniques (flo-by, mask, personal oxygen device, etc) – O2 administration should not increase the patient’s O2 requirements!
In cases of advanced hypoxemia, where mechanical ventilation is not feasible, nasotracheal O2 administration has proven to be helpful. By filling the majority of the upper airways with O2 between each breath, FiO2 increases. Placement of a nasotracheal catheter requires a very brief period of anesthesia with O2 administration throughout the procedure being paramount. Alternatively a transtracheal catheter is an option, but limits the rate of O2 supplementation due to smaller catheter sizes.
Lastly, the absence of cyanosis does not mean lack of O2 deprivation. The sensitivity of cyanosis to O2 deprivation is dependent on the RBC mass of the patient.
Feline urethral obstructions are an emergency disorder that may have catastrophic results if a proper protocol is not followed. Initiation of monitoring procedures is paramount for early detection of complications. The following protocol is advised by the author:
1. Analgesic administration, shave for IV catheter and initial chlorhexidine scrub, pending owner decision to treat.
2. Place IV catheter.
3. Use stylet to obtain blood for PCV/TS and I-stat (blood gas, lytes, BUN) or equivalent.
a. Consider phlebotomy for CBC and chemistry (ideally a creatinine at a minimum)
4. IV fluids with balanced electrolyte solution (Normosol-R, Plasmalyte-R, LRS).
a. 0.9% saline is acidifying (low pH and high Cl-)
5. If hyperkalemia is sufficient to cause arrhythmias, poor perfusion, or altered mental status, then:
a. Administer regular insulin 0.2 units/kg IV followed by 2 gm dextrose (4 mls, 50% solution)/unit of insulin; maintain on 2.5% dextrose solution
b. Consider 10% calcium gluconate 1 ml/5-7 kg, IV slowly while monitoring ECG
c. Consider NaHCO3 if severe metabolic acidosis
6. Once arrhythmia is properly controlled, induction of anesthesia (if required). Avoid ketamine if a murmur or gallop rhythm is ausculted. Consider benzodiazepine, followed with etomidate or propofol.
7. Shave perineal region, sterile preparation.
8. Unblock urethra.
a. Massage penis to loosen crystalline / mucinous plug
b. Use 3.5 Fr closed-end (less preferably open-end) tom cat catheter and sterile electrolyte solution to back flush the obstruction
c. Consider cystocentesis to limit back pressure
d. For urethral spasms or swelling causing difficulty, consider:
i. 0.2% lidocaine for flush
ii. 0.25-0.5 mg/kg dexamethasone IV
9. Flush bladder and urethra thoroughly.
10. Place 3.5 Fr soft (red rubber or argyle) catheter, secure in place (stay sutures in prepuce, butterfly tape on catheter should run parallel, not perpendicular to catheter; tape adhered all the way around IV line, then to tail). Small catheter helps limit iatrogenic urethral spasms.
11. Attach catheter to a closed collection system and place E-collar on patient.
12. Prophylactic antibiotics not advised, actually perpetuate development of resistance; therapeutic antibiotics initiated if infection is evident on urinalysis or patient is severely debilitated.
13. Measure urine output and monitor PCV/TS, glucose, BUN and electrolytes as indicated.
14. Consider culture of urine at the time of catheter removal.
15. Flush urethra again at the time of catheter removal.
If attempts at urethral catheterization are unsuccessful, and a urethral tear is suspected, try to perform a retrograde urethral catheterization. Retrograde urethral catheterization consists of a cystocentesis with peripheral IV catheter, placement of an antegrade stylet (through percutaneous catheter into the urinary bladder and out the urethra), followed by retrograde passage of a urethral catheter over the stylet and into the urinary bladder.
The default is to provide O2 administration unless insufficient hands available to maintain this while providing other therapies. Avoid nasal line placement if nasal or skull fractures are suspected or if stimulates sneezing or head shaking. Avoid excessive manipulation of the head and neck, bilateral jugular vein occlusion or allowing the head to fall below the level of the heart at anytime.
Peripheral IV catheter should be placed with initial data base (PCV/TS, BC, plasma, BUN, glucose, electrolytes and blood gas). Preferred fluid is physiologic saline ± hypertonic saline. Lactated Ringers solution is less optimal due to an increase in free water. Dextrose solutions should be avoided due to free water (D-5-W) and/or to limit hyperglycemia.
Physical exam with extensive, serial neurologic assessment should be performed. Baseline blood pressure is strongly encouraged. It is vital to provide appropriate volume replacement and stabilization with neurologic assessment prior to mannitol administration. The latter can cause a marked osmotic diuresis, which may compromise cerebral perfusion further. It is generally agreed to avoid the administration of glucocorticoids.
Mild hypothermia may be preferred – do not aggressively rewarm or overheat patients, limiting cerebral metabolic rate and O2 requirements. If PaCO2 is >45 mmHg, intubate and provide positive pressure ventilation. Treat seizures with diazepam, propofol and/or pentobarbital – intubate if gag reflex is lost.
Presumably under the influence of adrenaline, there is a significant tendency to over-ventilate CPR patients. It is not uncommon for trained health care workers to be observed ventilating cardiopulmonary arrest (CPA) patients at 20-30 breaths/min (bpm), despite the current recommendations of 8-10 bpm. These manual respirations, unlike spontaneous breathing, inflate the lungs by providing positive intrathoracic (IT) pressure. This increase in IT pressure deleteriously impedes venous return to the thorax, and thus decreases ventricular filling. Inadequate ventricular filling limits the ability of chest compressions to provide sufficient cardiac output in this no or low-flow state. High IT pressures can also reduce coronary perfusion pressure (see below). It is not only elevated respiratory rates, but also increased tidal volumes that may be deleterious. It is important to know that pediatric AMBU bags and adult AMBU bags have tidal volumes of 450-500 mls and 1100-1600 mls, respectively.
Experimental data suggests that as little as 10s of interruption to chest compression compromises patient outcomes. There are many maneuvers that may detract from the performance of chest compressions, including attaching monitors, endotracheal intubation, defibrillation, rhythm evaluation, establishing vascular access, medication administration (if endotracheal) and ventilations in out-of-hospital resuscitation attempts. It should be emphasized therefore, that these maneuvers be performed in a rapid, efficient manner to minimize interruptions in chest compression. For this same reason, it should be no longer recommended to stop chest compressions to deliver manual respirations.
If an IV or IO catheter is not available, the endotracheal (ET) route should be used. The medications that can be given via the ET route, include the NAVEL drugs; naloxone, atropine, vasopressin, epinephrine, and lidocaine. Blood levels of drugs given by the ET route are lower than comparable blood levels when drugs are given intravenously. The optimal dose of ET-administered medications is unknown, but generally should be given 2 to 2.5 times greater than the IV dose, with some studies suggesting the required dose of epinephrine given ET should be 3 to 10 times higher than the equipotent IV dose. The administered ET medications should be given with up to 10 mls of sterile water and flushed with several brisk ventilations. Sterile water has been shown to be superior to sterile saline in some studies.
Electrolytes are commonly excluded in the basic biochemical evaluation of vomiting patients. Not only does their inclusion help evaluate for alterations that occur due to gastric fluid losses, but it also helps evaluate for hypoadrenocorticism, as well as evidence of an upper GI obstruction. The latter is strongly suspected when a hypochloremic metabolic alkalosis is present. This not only helps the clinician diagnostically, but also provides justification for using 0.9% saline as the initial replacement and maintenance fluid to be administered. The presence of hypokalemia also should be therapeutically addressed to limit development of an ileus. The latter will further contribute to nausea and vomiting.
Nasoesophageal (NE) tubes are typically the temporary feeding tube of choice for provision of enteral nutrition only. Since NE tubes do not breach the lower esophageal sphincter they limit the risk of gastroesophageal reflux. Nasogastric (NG) tubes may be utilized in patients with ileus or complete GI obstruction, that are vomiting large volumes of fluid, to therapeutically decompress the stomach, minimizing the frequency and severity of vomiting. Specific patients that the author frequently relies on NG tubes to limit gastric fluid volumes are post-operative GDV, pancreatitis or parvoviral enteritis patients.
Nasointestinal tubes may be used for post-operative nutrition, especially if one is uncomfortable placing or maintaining enterostomy tubes. As with enterostomy tubes, nasointestinal tubes require a continuous infusion of a liquid nutritional product. Accidental or premature removal doesn't pose risk for peritonitis.
When treating a patient with clinical hypoglycemia, always give an initial dextrose bolus, followed by a supplemental infusion of dextrose until the patient proves they no longer need this supplementation. Please keep in mind that a low BG measurement on a glucometer can occur if the patient has a relative or absolute polycythemia. This inherent "error" can sometimes be avoided by performing a glucose measurement on plasma, instead of whole blood.
If a large breed dog presents with acute collapse and physical examination reveals pale pink mucous membranes and no palpable abdominal mass or effusion and/or mucous membrane cyanosis is present, think pericardial effusion! The patient is almost certain to have pericardial effusion if thoracic radiographs are normal and no appreciable upper airway noise is present. The other major differential is a pulmonary thromboembolism.
A normal blood pressure does not rule out a patient from being in shock. Oscillometric measurements require more specific cuff placement because the cuff is sensing the vibrations. As such, patient movement can cause erroneous readings. Patient's heart rate must correspond with the rate obtained by the blood pressure unit.
It is the author's experience that the clinical significance of hypoalbuminemia appears underappreciated. Plasma transfusion is a very inefficient means of replacing albumin. Synthetic colloids and/or human albumin products are preferred. It takes an estimated 45 ml/kg of plasma to raise the serum albumin by 1.0 mg/dl.
Always draw sample for EG semi-quantitative analysis before administering any activated charcoal. Activated charcoal commonly contains propylene glycol, which cross-reacts with EG testing.
Blood type all cats, dogs not so much if only DEA 1.1 negative blood products are available.
A Coombs may be useful for helping to diagnose an immune-mediate hemolytic anemia, but is useless in the diagnosis of immune-mediated thrombocytopenia. Not necessary in IMHA if spherocytosis present.
Select injectable vitamin K products may cause allergic reactions. Administration of injectable vitamin K is not necessary for successful treatment of most asymptomatic vitamin-K antagonist rodenticide ingestions. Oral vitamin K formulations are better absorbed than injectable formulations, in the absence of recent activated charcoal administration.
Activated charcoal is commonly administered to limit absorption of select toxins that remain in the stomach or intestines following emesis induction. Keep in mind that medications administered orally, as part of the therapeutic plan for patients having recently received activated charcoal, may be of limited benefit due to their absorption by the activated charcoal. Injectable formulations, if available, are advised until the patient has eaten a meal, which effectively provides a "barrier" between the therapeutic medication and the activated charcoal
Podcast CE: A Surgeon’s Perspective on Current Trends for the Management of Osteoarthritis, Part 1
May 17th 2024David L. Dycus, DVM, MS, CCRP, DACVS joins Adam Christman, DVM, MBA, to discuss a proactive approach to the diagnosis of osteoarthritis and the best tools for general practice.
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